Rifabutin in the treatment of cavitary lung disease due to Mycobacterium gordonae.

We have described a case of progressive pulmonary disease caused by M gordonae that failed to show any improvement in disease status after 9 months of intensive therapy with a conventional four-drug regimen. When rifabutin became available and was included in the regimen, the disease was cured. Although considered a saprophyte of the respiratory tract, M gordonae can cause clinically significant disease in rare instances. Initiation of appropriate therapy with rifabutin and other antituberculous agents could prevent the destructive lesions and prolonged morbidity of patients with disease caused by M gordonae.

"Ring around the artery" as a presenting feature in undiagnosed asthma with pneumomediastinum.

Acute bronchial asthma may be complicated by pneumomediastinum, often accompanied by the "ring around the artery" sign, described in association with asthma, trauma (gunshot wound), subclavian catheterization, and cocaine use, or with no identifiable risk factors. The diagnosis of pneumomediastinum should always be considered in an asthmatic patient with chest pain, cough, and dyspnea. Lateral chest film reveals a radiolucency outlining the right pulmonary artery. Such patients recover spontaneously with conservative therapy.

Psittacosis pneumonia.

A 57-year-old man with symptoms and signs consistent with atypical pneumonia had epidemiologic and later serologic evidence of psittacosis pneumonia. Therapy with tetracycline resulted in rapid resolution.

Diagnosis of pulmonary strongyloidiasis by bronchoalveolar lavage.

Bronchoalveolar lavage was performed on a patient with disseminated strongyloidiasis and 4.5 X 10(7) cells/65 ml of lavage fluid were recovered. Eighty-five percent of cells were polymorphonuclear leukocytes; 15 percent were pulmonary alveolar macrophages. Rhabditiform larvae (1 X 10(4)) were recovered in 65 ml of lavage fluid. This is the first report of bronchoalveolar lavage used in diagnosing disseminated strongyloidiasis.

Pulmonary strongyloidiasis. Diagnosis by sputum gram stain.

Sputum Gram stain was diagnostic for pulmonary strongyloidiasis in four patients from Tennessee with chronic obstructive lung disease treated with steroids. The case reports of these patients and photomicrographs of the larval forms by Gram stain are presented. Sputum Gram stain may be a useful procedure to screen for pulmonary strongyloidiasis in steroid-treated patients with chronic lung disease who come from an endemic area.

Inactivation of human bronchial mucosal proteinase inhibitor by Pseudomonas aeruginosa elastase.

Human bronchial mucus contains an acid-stable proteinase inhibitor called bronchial mucous inhibitor (BMI) that apparently protects the upper airways from proteolysis by polymorphonuclear leukocyte (PMN) elastase and cathepsin G, and infections of Pseudomonas aeruginosa, which also produces an elastase, can result in considerable lung damage. The possible role of BMI in protecting the lung from proteolytic attack in the presence of P. aeruginosa elastase (a zinc metalloprotease) was investigated. The BMI not only failed to inhibit P. aeruginosa elastase but the ability of BMI to inhibit PMN elastase and cathepsin G was rapidly lost in the presence of the bacterial elastase. The P. aeruginosa elastase also freed active PMN elastase from complexes with BMI, resulting in elastin digestion by both enzymes. The proteolysis of lung tissue observed with P. aeruginosa infections may be caused by a combination of bacterial and PMN proteases. Elastase and cathepsin G released from leukocytes, attracted to P. aeruginosa infection sites, would be free to attack the bronchial tissues after BMI inactivation by P. aeruginosa elastase, adding to the damage caused by the bacterial protease(s).

Inflammatory reaction and airway damage in cystic fibrosis.

In cystic fibrosis there is chronic infection and inflammatory reaction in the airways, accompanied by destruction and shedding of airway epithelium. Leukocytes migrate into the airways and some disintegrate, liberating deoxyribonucleoprotein that is incorporated into the gel structure of the bronchial mucus. We compared the status of these processes in cystic fibrosis with that in chronic bronchitis and bronchiectasis, by examining the sputum raised from the lower airways. Measurements also were made on sputum induced in normal subjects. The results indicate that migration of leukocytes into the airways and shedding of damaged airway epithelium were minimal in the normal subjects; they were significant in the patients with chronic bronchitis, higher in those with bronchiectasis, and still higher in those with cystic fibrosis. The large increases found in the total content of DNA and solids in the cystic fibrosis sputum were due to increases in the insoluble fraction containing the whole leukocytes and particulate debris that remained when the sputum mucus gel was solubilized with mercaptoethanol. Despite the large increases in the total content of DNA and solids, the contents of mucus gel components and of deoxyribonucleoprotein from disintegrated leukocytes actually present in the mucus gel structure of the cystic fibrosis sputum were not significantly higher than in the sputum from the patients with chronic bronchitis or brochiectasis.